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Titolo:
Calmodulin kinases II and IV and calcineurin are involved in leukemia inhibitory factor-induced cardiac hypertrophy in rats
Autore:
Kato, T; Sano, M; Miyoshi, S; Sato, T; Hakuno, D; Ishida, H; Kinoshita-Nakazawa, H; Fukuda, K; Ogawa, S;
Indirizzi:
Keio Univ, Sch Med, Dept Internal Med, Cardiopulm Div,Shinjuku Ku, Tokyo 1608582, Japan Keio Univ Tokyo Japan 1608582 pulm Div,Shinjuku Ku, Tokyo 1608582, Japan Tokai Univ, Dept Physiol, Kanagawa 2591100, Japan Tokai Univ Kanagawa Japan 2591100 Dept Physiol, Kanagawa 2591100, Japan
Titolo Testata:
CIRCULATION RESEARCH
fascicolo: 10, volume: 87, anno: 2000,
pagine: 937 - 945
SICI:
0009-7330(20001110)87:10<937:CKIAIA>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
ATRIAL-NATRIURETIC-FACTOR; VENTRICULAR MYOCYTES; GENE-EXPRESSION; CALCIUM INFLUX; MICE; CARDIOMYOCYTES; ACTIVATION; CELLS; CYCLOSPORINE; STIMULATION;
Keywords:
leukemia inhibitory factor; calcium; calmodulin-dependent kinase; calcineurin; cardiac hypertrophy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Fukuda, K Keio Univ, Sch Med, Dept Internal Med, Cardiopulm Div,Shinjuku Ku, 35 Shinanomachi, Tokyo 1608582, Japan Keio Univ 35 Shinanomachi Tokyo Japan 1608582 yo 1608582, Japan
Citazione:
T. Kato et al., "Calmodulin kinases II and IV and calcineurin are involved in leukemia inhibitory factor-induced cardiac hypertrophy in rats", CIRCUL RES, 87(10), 2000, pp. 937-945

Abstract

We recently reported that leukemia inhibitory factor (LIF) enhances Ca2+](i) through an increase in L-type Ca2+ current (I-Ca,I-L) in adult cardiomyocytes. The aim of this study was to investigate whether LIF activates Ca2+-dependent signaling molecules, such as calcineurin and calmodulin kinases II and IV (CaMKII and CaMKIV), and, if so, whether these Ca2+-mediated signaling events contribute to LIF-mediated cardiac hypertrophy. We first confirmed that LIF increased I-Ca,I-L and [Ca2+](i) in primary cultured rat neonatal cardiomyocytes. Calcineurin, CaMKII, and CaMKIV activities increased at2 minutes and peaked by 1.6-, 2.2-, and 2.2-fold, respectively, at 15 minutes. Nicardipine or verapamil fully inhibited these activities. Autophosphorylation of CaMKII was also observed to parallel the timing of CaMKII activity, and this phosphorylation was blocked by nicardipine, verapamil, or EGTA. LIF treatment led to a 3-fold increase in nuclear factor of activated T cell-luciferase activity. To confirm that inositol triphosphate (IP3)-induced Ca2+ release from sarcoplasmic reticulum was not involved in this process, IP3 content and phosphorylation of phospholipase C gamma were investigated. LIF did not increase IP3 content or phosphorylate phospholipase C gamma. KN62 (an inhibitor of CaMKII and CaMKIV) attenuated c-fos, brain natriuretic peptide, alpha -skeletal actin, and atrial natriuretic peptide expression. KN62 suppressed the LIF-induced increase in [H-3]phenylalanine uptake and cell size. Cyclosporin A and FK506 slightly attenuated brain natriureticpeptide but did not affect c-fos or atrial natriuretic peptide expression. Cyclosporin A significantly reduced the LIF-induced increase in [H-3]phenylalanine uptake. These findings indicated that LIF activated CaMKII, CaMKIV, and calcineurin through an increase in I-Ca,I-L and [Ca2+](i) and that CaMKII, CaMKIV, and calcineurin are critically involved in LIF-induced cardiac hypertrophy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 21:40:08